Anti-ATG7

Formulation: Phosphate-buffered saline (PBS) with 50% glycerol, 0.5% BSA and 0.09% sodium azide. Identity-Mouse (%): 90%. Homologies: Highest antigen sequence identity to the following orthologs: Mouse - 90%, Rat - 91%, Pig - 92%, Cynomolgus monkey - 99%. IHC Verification: succeed. WB Verification: -. IP Verification: -. IF Verification: -. FC Verification: -. IP-MS Verification: -. Cross reactivity: Not tested. Sandwich ELISA Verification: -. Antigen ID: ABS-PP-4697. Core Sequence: SKLQFAPFSS ALDVGFWHEL TQKKLNEYRL DEAPKDIKGY YYNGDSAGLP ARLTLEFSAF DMSAPTPARC CPAIGTLYNT NTLESFKTAD KKLLLEQAAN EIWESIKSGT ALENPVLLNK FLLLTFADLK KYHFYYWFCY PALCLPESLP LIQGPVGLDQ RFSLKQIEAL ECAYDNLCQT EGVTALPYFL IKYDENMVLV SLLKHYSDFF QGQRTKITIG VYDPCNLAQY PGWPLRNFLV LAAHRWSSSF QSVEVVCFRD RTMQGARDVA HSIIFEVKLP EMAFSPDCPK AVGWEKNQKG GMGPRMVNLS ECMDPKRLAE. Recombinant Antibody: Protein Function: E1-like activating enzyme involved in the 2 ubiquitin-like systems required for cytoplasm to vacuole transport (Cvt) and autophagy. Activates ATG12 for its conjugation with ATG5 as well as the ATG8 family proteins for their conjugation with phosphatidylethanolamine. Both systems are needed for the ATG8 association to Cvt vesicles and autophagosomes membranes. Required for autophagic death induced by caspase-8 inhibition. Facilitates LC3-I lipidation with phosphatidylethanolamine to form LC3-II which is found on autophagosomal membranes (PubMed:34161705). Required for mitophagy which contributes to regulate mitochondrial quantity and quality by eliminating the mitochondria to a basal level to fulfill cellular energy requirements and preventing excess ROS production. Modulates p53/TP53 activity to regulate cell cycle and survival during metabolic stress. Also plays a key role in the maintenance of axonal homeostasis, the prevention of axonal degeneration, the maintenance of hematopoietic stem cells, the formation of Paneth cell granules, as well as in adipose differentiation. Plays a role in regulating the liver clock and glucose metabolism by mediating the autophagic degradation of CRY1 (clock repressor) in a time-dependent manner (By similarity) [The Uniprot Consortium]